Immunohistochemical characterisation of dendritic cells in human atherosclerotic lesions: possible pitfalls

Vré, Emily A. Van; Bosmans, Johan; Brussel, Ilse Van; Maris, Mieke; Meyer, Guido R.Y. De; Schil, Paul E. Van; Vrints, Christiaan J.; Bult, Hidde

doi:10.1097/pat.0b013e328344e266

Cited by 35 publications

(37 citation statements)

References 30 publications

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“…Unfortunately, attempts to visualize DC subtype markers (CD80, CD86, DC lamp, and DC sign) failed on formalin‐fixed, paraffin‐embedded material, as demonstrated in a previous study 39. As such, DCs could only be recognized by the general DC marker, fascin, which has been shown to correlate with DC maturation into APCs 40…”

Section: Discussionmentioning

confidence: 97%

Systematic Evaluation of the Cellular Innate Immune Response During the Process of Human Atherosclerosis

Dijk

Rijs

Wezel

et al. 2016

JAHA

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BackgroundThe concept of innate immunity is well recognized within the spectrum of atherosclerosis, which is primarily dictated by macrophages. Although current insights to this process are largely based on murine models, there are fundamental differences in the atherosclerotic microenvironment and associated inflammatory response relative to humans. In this light, we characterized the cellular aspects of innate immune response in normal, nonprogressive, and progressive human atherosclerotic plaques.Methods and ResultsA systematic analysis of innate immune response was performed on 110 well‐characterized human perirenal aortic plaques with immunostaining for specific macrophage subtypes (M1 and M2 lineage) and their activation markers, neopterin and human leukocyte antigen–antigen D related (HLA‐DR), together with dendritic cells (DCs), natural killer (NK) cells, mast cells, neutrophils, and eosinophils. Normal aortae were devoid of low‐density lipoprotein, macrophages, DCs, NK cells, mast cells, eosinophils, and neutrophils. Early, atherosclerotic lesions exhibited heterogeneous populations of (CD68+) macrophages, whereby 25% were double positive “M1” (CD68+/ inducible nitric oxide synthase [iNOS]+/CD163−), 13% “M2” double positive (CD68+/iNOS −/CD163+), and 17% triple positive for (M1) iNOS (M2)/CD163 and CD68, with the remaining (≈40%) only stained for CD68. Progressive fibroatheromatous lesions, including vulnerable plaques, showed increasing numbers of NK cells and fascin‐positive cells mainly localized to the media and adventitia whereas the M1/M2 ratio and level of macrophage activation (HLA‐DR and neopterin) remained unchanged. On the contrary, stabilized (fibrotic) plaques showed a marked reduction in macrophages and cell activation with a concomitant decrease in NK cells, DCs, and neutrophils.ConclusionsMacrophage “M1” and “M2” subsets, together with fascin‐positive DCs, are strongly associated with progressive and vulnerable atherosclerotic disease of human aorta. The observations here support a more complex theory of macrophage heterogeneity than the existing paradigm predicated on murine data and further indicate the involvement of (poorly defined) macrophage subtypes or greater dynamic range of macrophage plasticity than previously considered.

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Section: Discussionmentioning

confidence: 97%

Systematic Evaluation of the Cellular Innate Immune Response During the Process of Human Atherosclerosis

Dijk

Rijs

Wezel

et al. 2016

JAHA

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“…For instance, mertyrosine kinase (MERTK) is cleaved under inflammatory conditions, and soluble MERTK can compete for the ligands of membrane bound MERTK and therefore impede efferocytosis. 52 Apart from macrophages, increased numbers of immature DCs are present in atherosclerotic lesions 53 and might also be implicated in efferocytosis in atherosclerosis. As recently discussed, 54 different efferocytes might have different effects on plaque evolution.…”

Section: Impaired Efferocytosis In Atherosclerosismentioning

confidence: 99%

Apoptotic Cell Death and Efferocytosis in Atherosclerosis

Vré

Ait‐Oufella

Tedgui

et al. 2012

ATVB

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“…In atherosclerosis, DCs are found in vascular plaques [45] and their function depends on their different subsets. While plasmacytoid DCs (pDCs) and tolerogenic DCs (tDCs) protect against atherosclerosis [46,47], CCL17 þ conventional DCs (cDCs) drive atherosclerosis [48], through the regulation of the balance of effector T-cells and Tregs.…”

Section: Discussionmentioning

confidence: 99%

Disruption of the TSLP-TSLPR-LAP signaling between epithelial and dendritic cells through hyperlipidemia contributes to regulatory T-Cell defects in atherosclerotic mice

Mao

Meng

et al. 2015

Atherosclerosis

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Immunohistochemical characterisation of dendritic cells in human atherosclerotic lesions: possible pitfalls

Cited by 35 publications

References 30 publications

Systematic Evaluation of the Cellular Innate Immune Response During the Process of Human Atherosclerosis

Systematic Evaluation of the Cellular Innate Immune Response During the Process of Human Atherosclerosis

Apoptotic Cell Death and Efferocytosis in Atherosclerosis

Disruption of the TSLP-TSLPR-LAP signaling between epithelial and dendritic cells through hyperlipidemia contributes to regulatory T-Cell defects in atherosclerotic mice

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